血浆置换治疗血栓性血小板减少性紫癜临床疗效的观察

目的观察血浆置换治疗血栓性血小板减少性紫癜的临床疗效。方法回顾分析2013年1月—2018年6月本院14例确诊为血栓性血小板减少性紫癜患者的临床特征及进行血浆置换治疗后的疾病转归情况,分析血浆置换治疗过程中不良反应发生情况。结果 14例血栓性血小板减少性紫癜患者共进行了47次血浆置换,经过血浆置换治疗后10例患者病情好转恢复出院,血浆置换治疗血栓性血小板减少性紫癜患者的总有效率为71.4%。47次血浆置换术中共发生了3次不良反应,其不良反应发生率为6.4%。结论血浆置换是治疗血栓性血小板减少性紫癜的有效方法,患者一旦确诊或高度怀疑为血栓性血小板减少性紫癜时需尽早开始血浆置换治疗。     

血浆置换治疗血栓性血小板减少性紫癜的临床疗效观察

选取2011年1月~2013年12月在我院就诊的且符合《血液病诊断及疗效标准》的血栓性血小板减少性紫癜患者8例纳入研究对象,予以其血浆置换治疗。对比治疗前与治疗6个月后患者的血小板计数(PLT)、血红蛋白(Hb)、尿素氮(BUN)、总胆红素(TBIL)、乳酸脱氢酶(LDH)的变化情况。结果给予患者血液置换治疗后,患者的血小板计数(PLT)、血红蛋白(Hb)明显增加,差异具有统计学意义(P<0.05);患者的尿素氮(BUN)、总胆红素(TBIL)、乳酸脱氢酶(LDH)明显降低,差异具有统计学意义(P<0.05)。有1例患者行3次治疗后复发,再次予以其2次血浆置换治疗后痊愈。有2例行3次血浆置治疗后痊愈,有2例行血浆置换治疗4次后痊愈,有3例行血浆置换治疗5次后痊愈。血浆置换在治疗血栓性血小板减少性紫癜有着良好的治疗效果,提高治疗的成功率和治愈率。     

血浆置换治疗血栓性血小板减少性紫癜14例护理体会

目的:探讨血浆置换治疗血栓性血小板减少性紫癜(TTP)的护理方法.方法:对14例TTP患者进行血浆置换治疗、出血的预防和护理、严密观察病情、感染的预防及护理、血浆置换护理.结果:本组患者住院7～28d,平均17.5d,其中1例因颅内出血死亡,其余13例均临床治愈出院.结论:针对血栓性血小板减少性紫癜起病急、发展迅猛、病死率高、护理难度大等特点,进行严密的观察和细致的护理,能降低患者病死率,有效地促进患者康复.     

冷上清在治疗血栓性血小板减少性紫癜中的应用

目的探讨冷上清在治疗血栓性血小板减少性紫癜中的临床应用价值。方法用冷上清做置换液,采用血浆置换疗法,对20例血栓性血小板减少性紫癜（TTP）患者进行治疗,判定治疗效果。结果20例TTP患者的治疗有效率达90％。结论冷上清做置换液对TTP患者进行血浆置换的疗效显著,且节约血液资源。     

整体护理干预对血栓性血小板减少性紫癜患者血浆置换的效果分析

目的 探讨整体护理干预对血栓性血小板减少紫癜患者血浆置换的护理效果.方法 选取2019年6月到2022年4月在我院进行治疗的以52例血栓性血小板减少紫癜患者作为研究对象.依据简单随机法将患者分成对照组和实验组,每组各26例.对照组采取常规护理方法,实验组采取整体护理干预.分析比较两组的检测指标、治疗效果、并发症情况、生活质量.结果 实验组在护理后的TBIL(总胆红素)、LDH(乳酸脱氢酶变化)、BUN(血尿素氮)显著高于对照组而Hb(血红蛋白)显著低于对照组(P<0.05).实验组的总有效率显著高于对照组     

血栓性血小板减少性紫癜合并肺孢子菌肺炎患者的护理

报道1例血栓性血小板减少性紫癜合并肺孢子菌肺炎患者的成功抢救与护理。本例患者是血栓性血小板减少性紫癜,经积极血浆置换和激素等治疗后好转,但由于长期使用激素,后合并肺孢子菌肺炎。其护理要点包括:监测生命体征,血浆置换的准备、操作和观察,预防出血和止血,采取各种措施预防感染,加强神经系统异常的护理,并注意患者和家属的心理疏导等。该患者经过医护人员精心治疗和护理,转危为安。     

血浆置换联合化疗、免疫抑制剂治疗噬血细胞综合症合并血栓性血小板减少性紫癜的临床观察

目的观察血浆置换联合化疗、免疫抑制剂治疗罕见病——噬血细胞综合征合并血栓性血小板减少性紫癜的疗效。方法 2014年1-3月对本科两例噬血细胞综合征合并血栓性血小板减少性紫癜患者采用血浆置换联合环孢素、糖皮质激素、足叶乙甙方案进行治疗,随访至2015年3月。结果 2例患者血常规均恢复正常,发热、精神症状消失,肾功能恢复正常,骨髓嗜血现象消失,至今存活。结论血浆置换联合化疗、免疫抑制剂是治疗噬血细胞综合征合并血栓性血小板减少性紫癜的有效方法。     

间接胆红素在血浆置换联合山莨菪碱治疗血栓性血小板减少性紫癜中的变化观察

目的观察间接胆红素（I-Bil）在山莨菪碱加血浆置换（PE）干预血栓性血小板减少性紫癜（TTP）的变化情况,以了解山莨菪碱在TTP干预中的效果。方法选择82例TTP患者随机分组,联合干预组41例予山莨菪碱加血浆置换（PE）,疗程21d;对照组41例单纯予以PE干预,疗程21d。结果联合干预组21d后有效率90.2%,对照组有效率82.9%,差异有显著性（P〈0.05）,I-Bil在干预后第2、5、12d数值下降速度明显快于对照组,差异有显著性（P〈0.05）,有统计学意义。结论血浆置换联合山莨菪碱注射液干预血栓性血小板减少性紫癜间接胆红素下降更快,疗效更好。     

1例血栓性血小板减少性紫癜的护理

报告1例血栓性血小板减少性紫癜的护理体会。主要内容包括：病情的观察护理,血浆置换的护理,用药护理,针对性心理护理,预防并发症等。本例患者经过32d的精心治疗护理,痊愈出院。     

血浆置换治疗血栓性血小板减少性紫癜6例的护理

总结6例血栓性血小板减少性紫癜行血浆置换治疗的护理。血浆置换前做好治疗用物准备及并发症预防处置;血浆置换时,安置患者舒适体位,建立有效的血管通路,做好出血、神经系统及血流动力学的观察与护理;血浆置换治疗结束正确拔针及按压。5例治愈出院,1例因未早期连续置换导致病情加重转院治疗。     

神经系统症状为首发表现的血栓性血小板减少性紫癜1例报告

<正>血栓性血小板减少性紫癜(TTP)是血液科急重症,根据"五联征"或"三联征"诊断并不困难。但此病临床上少见,大多急骤起病、进展快、病情凶险、缺乏特异性临床症状和体征,容易误诊、漏诊。本病例以中枢神经系统症状为首发表现,首先考虑为脑膜脑炎或脑血管病等神经系统疾病,且患者合     

血栓性血小板减少性紫癜2例报道

目的总结兰州大学第二医院2例血栓性血小板减少性紫癜(TTP)的所有实验检测资料。方法回顾性分析与TTP诊断特征密切相关的实验室检测:血红蛋白(Hb)、血小板(PLT)、网织红细胞(RET)、裂片红细胞(FRC)、尿蛋白(PRO)、尿潜血(BLD)、乳酸脱氢酶(LDH)、总胆红素(TBil)、直接胆红素(DBil)、间接胆红素(IBil)、尿素氮(BUN),肌酐(Cr)、D二聚体(D-D)及骨髓检测,并归纳分析。结果血浆、PLT、静丙输注无法改善PLT的严重减少;输注红细胞(RBC),Hb进行性下降;尿液PRO及BLD定性持续阳性;溶血检测中的RET、TBil、IBil及LDH持续增高;凝血检测中D-D持续不降;骨髓分析提示2例患者分别是增生性贫血与溶血性贫血并考虑Evans综合症。结论对于TTP浅显认识导致临床诊治延误。回顾性总结TTP实验室检测及临床特征,发现有经典"五联征",包括血小板减少症、微血管病性溶血性贫血、神经症状、肾脏损害及发热。     

Early plasmapheresis in patients with thrombotic thrombocytopenic purpura.

OBJECTIVES: To investigate the relationship of thrombotic thrombocytopenic purpura to adult respiratory distress syndrome (ARDS) and study the responses of thrombotic thrombocytopenic purpura patients to early plasmapheresis. DESIGN: Case series. SETTING: ICU of a university hospital. PATIENTS: Twenty-four consecutive patients with thrombotic thrombocytopenic purpura, with various periods of time (1 to 18 days) having elapsed since the onset of this condition. Patients ranged in age from 17 to 66 yrs. INTERVENTIONS: Plasmapheresis, using intermittent flow separators, was instituted soon after the patients' ICU admission. The retinoscopic findings on admission and the relationship of Pao2 to platelet counts before and after plasmapheresis therapy were recorded. Antiplatelet agents were given to the survivors to prevent relapses. MEASUREMENTS AND MAIN RESULTS: Eighteen patients survived and six died. Plasmapheresis was administered for a range of 1 to 5 days (mean 3) and 3 to 18 days (mean 9.8) in survivors and nonsurvivors, respectively (p less than .001). Four patients with confluent fundus hemorrhages died and seven without these fundoscopic findings had easily controlled disease. Increases in Pao2 paralleled increases in platelet counts after plasmapheresis (p less than .001) in this small series of patients. Three of 18 discharged survivors relapsed over a period of 3 to 56 months of follow-up. CONCLUSIONS: Early introduction of plasmapheresis in thrombotic thrombocytopenic purpura seems to increase the survival rate and to halt the development of ARDS. Fundus findings may be a prognostic factor in thrombotic thrombocytopenic purpura. The antiplatelet agents seem to be efficacious in the prevention of relapses.     

Plasmapheresis for thrombotic thrombocytopenic purpura (TTP)

A 70-year-old woman with thrombotic thrombocytopenic purpura (TTP) was treated with plasmapheresis using fresh frozen plasma as a fluid replacement. Complete recovery and lasting remission were observed. It appears that plasmapheresis combined with massive fresh frozen plasma can be an effective mode of treatment for patients who were, otherwise, refractory to conventional therapy.     

Idiopathic thrombocytopenic purpura during remission of thrombotic thrombocytopenic purpura

Three patients were treated empirically with anti-platelet agents, prednisone, plasmapheresis, and prostacyclin for the classical clinical syndrome of thrombotic thrombocytopenic purpura (TTP). All three patients initially responded, then relapsed after one to 13 months with a clinical picture characteristic of immunogenic thrombocytopenic purpura (ITP). At relapse, all three had thrombocytopenia without microangiopathy or other causes of thrombocytopenia. All responded to splenectomy. This complication of TTP may become more common with improved survival in TTP. Recognition may prevent inappropriate therapy.     

Resolution of refractory, classic thrombotic thrombocytopenic purpura after staphylococcal protein A immunoadsorption

BACKGROUND: Multiple therapeutic interventions are available for treatment of thrombotic thrombocytopenic purpura. Resolution of thrombotic thrombocytopenic purpura may require use of several of these interventions. CASE REPORT: A patient presenting with classic (non- cancer chemotherapy-associated) thrombotic thrombocytopenic purpura had an initial response to intensive, daily plasma exchange with fresh- frozen plasma and cryosupernatant. Multiple attempts over a period of 2 months to decrease the frequency of plasma exchange resulted in exacerbations of disease activity, indicated by increased schistocytosis, decreased hematocrit, increased serum lactate dehydrogenase, and decreased platelet counts. After a total of 39 plasma exchanges, the patient was begun on immunoadsorption therapy utilizing a staphylococcal protein A immunoadsorption treatment column. After six 2000-mL protein A immunoadsorption treatments, the patient's platelet count, lactate dehydrogenase, and peripheral smear normalized, and they have remained normal over nearly 4 months of follow-up. CONCLUSION: Treatment by protein A immunoadsorption may be of benefit in patients with classic thrombotic thrombocytopenic purpura who are not achieving a sustained remission with conventional plasma exchange therapy.     

Thrombotic thrombocytopenic purpura: successful treatment unlocks etiologic secrets

The cause of platelet agglutination in thrombotic thrombocytopenic purpura has been an enigma. Current evidence indicates that the interaction of platelets with a platelet-aggregating factor or unusually large multimers of factor VIII: von Willebrand factor, or both, may cause the abnormal platelet agglutination. Recent success in the treatment of thrombotic thrombocytopenic purpura with intravenous infusion of immunoglobulin suggests that the abnormal platelet agglutination in thrombotic thrombocytopenic purpura may reflect a deficiency of immunoglobulins that normally inhibit platelet-aggregating factors or large multimers of factor VIII: von Willebrand factor.     

Eradication of Helicobacter pylori increases platelet count in patients with idiopathic thrombocytopenic purpura in Japan

BACKGROUND: The effect of Helicobacter pylori eradication on the platelet count in patients with thrombocytopenic purpura is controversial. In this multicentre study, we prospectively assessed the effect of H. pylori eradication therapy in idiopathic thrombocytopenic purpura patients. MATERIALS AND METHODS: Thirty-five consecutive patients with chronic idiopathic thrombocytopenic purpura (11 males and 24 females, a median age of 57) were assessed for H. pylori infection by use of a urea breath test. All patients received 1-week triple therapy (amoxicillin, clarithromycin, and lansoprazole) to eradicate H. pylori. At 6 months, idiopathic thrombocytopenic purpura patients with a platelet count recovery of greater than 100 x 10(9) L(-1) were defined as idiopathic thrombocytopenic purpura responders. RESULTS: Helicobacter pylori infection was observed in 25 (71%) of the 35 patients. All infected patients were cured. Eleven patients were identified as idiopathic thrombocytopenic purpura responders; 24 were considered nonresponders. Platelet counts improved by more than 100 x 10(9) L(-1) in 11 (44%) of the 25 patients cured of H. pylori infection, while none of the 10 patients H. pylori-negative patients experienced the same improvement (P = 0.015). Univariate analysis showed that H. pylori infection and its eradication were significant factors associated with platelet recovery (P = 0.015). CONCLUSIONS: Helicobacter pylori infection played a role in the pathogenesis of idiopathic thrombocytopenic purpura in approximately 30% of all patients assessed and 45% of the patients with H. pylori infection. Eradication of H. pylori in idiopathic thrombocytopenic purpura patients led to improved disease activity.     

Increased troponin I is associated with fatal outcome in acquired thrombotic thrombocytopenic purpura

Thrombotic thrombocytopenic purpura (TTP) has >90% mortality without therapeutic plasma exchange (TPE). Despite TPE, approximately 10% of patients still die, presumably from cardiac ischemia. We sought clinical or laboratory parameters associated with death by reviewing the records of all patients hospitalized with acquired TTP in our institution for 10 years, and collect demographics and results for hemoglobin, platelet count, creatinine, lactate dehydrogenase, transaminases, total bilirubin, creatinine kinase (CK), CK‐MB, and troponin I. Sixty‐eight patients were admitted 88 times, and 11 died. Survivors and non‐survivors were similar in terms of sex, ethnicity, thrombocytopenia, and degree of anemia at presentation, while the latter were older, had worse renal function and higher CK, CK‐MB, and troponin I (univariate analysis). However, only troponin I remained significant on multivariate analyses. We propose that patients with TTP should be monitored with troponin I to detect significant myocardial ischemia that could predict death despite TPE.